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Host-dependent restriction of mengovirus replication
Abstract:
Mengovirus infection of a restrictive cell line, Maden's bovine kidney (MDBK), results in a virus yield 1,000-fold less than that obtained from productively infected cell lines such as L cells or Ehrlich ascites tumor cells (EAT). Cells of both types of host systems are infected with comparable efficiencies and are completely killed as a consequence of infection. Infective center assays, coupled with the observation of total cell killing, suggest that comparable numbers of cells synthesize viral antigen and release virus in both types of host system. Viral-specific ribonucleic acid (RNA) synthesis is initiated and proceeds in an identical fashion for approximately 4 hr after the infection of MDBK, EAT, or L-cells. At this time, viral RNA synthesis in MDBK ceases, whereas viral RNA synthesis in EAT and L-cells continues at a linear rate. These results indicate that none of the early viral events leading to the initiation of viral-specific RNA synthesis constitutes the primary site of mengovirus restriction in MDBK. Rather it appears that the cessation of viral RNA synthesis in restrictive cells constitutes the primary limiting event. Based on its delayed interaction with mengovirus RNA synthesis, it appears that the host-related restrictive agent is initially compartmentalized and then released as a consequence of infection subsequent to those early events in mengovirus infection leading to the initiation and continued synthesis of viral RNA.
Insights
Mengovirus infection is restricted in MDBK cells due to a halt in viral RNA synthesis. This host-related factor appears compartmentalized, impacting viral replication later in infection.
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Mengovirus infection yields are significantly lower in restrictive Madin-Darby Bovine Kidney (MDBK) cells compared to productive L cells or Ehrlich ascites tumor cells (EAT).
- Despite reduced yield, MDBK cells are infected with similar efficiency and undergo complete cell killing, indicating early viral events are not the primary restriction point.
Purpose of the Study:
- To investigate the molecular mechanisms underlying mengovirus restriction in MDBK cells.
- To identify the specific stage of viral replication where mengovirus is limited in restrictive host cells.
Main Methods:
- Comparative analysis of mengovirus replication in MDBK, L, and EAT cells.
- Infective center assays to assess viral antigen synthesis and release.
- Quantification of viral-specific RNA synthesis over time post-infection.
Main Results:
- Viral RNA synthesis initiates and proceeds similarly in all cell types for approximately 4 hours.
- Viral RNA synthesis ceases in MDBK cells at the 4-hour mark, while continuing linearly in EAT and L cells.
- Comparable numbers of cells synthesize viral antigen and release infectious virus in both restrictive and productive systems.
Conclusions:
- The primary restriction of mengovirus in MDBK cells is not due to early infection events but rather the cessation of viral RNA synthesis.
- A host-related restrictive factor appears to be released later in the infection process, subsequent to the initiation of viral RNA synthesis.